Adrenal disorders

Dr Mona Mashayekhi MD, PhD

Overview of adrenal insufficiency

	ACTH	Cortisol	Aldosterone	Renin	DHEA	Na	K	ACTH stim
Primary	high	low	low	high	low	low	high	nonreactive
Central	low	low	wnl	wnl	low-normal*	low**	wnl	reactive $

* DHEA has some response to ACTH

** via DDAVP, less extreme hypoNa compared to primary

$ if longstanding central process, ACTH stim will not be normal d/t atrophy

Sheehan - ACTH zero, cortisol zero, ACTH stim will be normal (no time yet for atrophy)

Primary adrenal insufficiency

post-op, infx, hemorrhage, mets, autoimmune

More electrolyte abnormalities d/t aldosterone problems (ENAC -> K up, Na down, also some vessel tonicity -> HoTN)

Secondary adrenal insufficiency (central)

E.g. chronic steroids (causes 1, 2, 3 of AI are iatrogenic d/t steroid use), Sheehans

ACTH cleaved to POMC, melanocortin -> hyperpigmentation (palms more specific)

Primary AI tx

Prefer hydrocortisone, as has short half-life and allows closer mimicry of physiologic levels. Higher AM dose, lower PM dose.

Relative half-lives and physiologic doses of steroids:

	dose	t ½
dex	0.25mg	+++
pred	4mg	++
hydro	?	+

Primary hyperaldosteronism

Common, should suspect if low K and resistant HTN.

Many BP meds modulate HPA axis in some way or another, practically only MRAs are considered sufficiently problematic to interfere with standard testing.

Start with aldo/renin ratio.

Primary hyperaldosteronism tx

Primary therapy is surgical.

MRA therapy can be helpful, but does not prevent other effect of unopposed aldosterone (e.g. cardiac), so preferred when pts are not surgical candidates.

For maximum effectiveness, titrate MRA dose to level of renin.

Adrenal venous sampling (AVS) - done by interventional radiology, highly specialized even within IR.

So some places, if <40yo, will just use CT evidence of nodule to justify removal. (if >40yo, high likelihood of benign adenoma)